Gestational Diabetes Mellitus (GDM) is defined as carbohydrate intolerance first recognized during pregnancy. According to the Diabetes in Pregnancy Study Group India (DIPSI), it can be diagnosed using a non-fasting Oral Glucose Tolerance Test (OGTT) with 75g glucose and a 2 hour cutoff of equal to or more than 140 mg per dl. GDM is a multifactorial condition involving both genetic and acquired factors affecting insulin sensitivity and secretion. Key contributors to its pathogenesis include altered maternal and placental hormones, inflammation, oxidative stress, and maternal adipokine changes, all leading to insulin resistance and reduced insulin secretion.

GDM creates a hypoxic placental environment that disrupts vascular development. Hypoxia stimulates Vascular Endothelial Growth Factor (VEGF) expression, leading to the release of VEGF, growth factors, C reactive protein, and plasma fibrinogen, which contribute to endothelial dysfunction and inflammation. VEGF, primarily produced by endothelial cells, promotes angiogenesis and vessel formation by binding to receptors VEGFR 1 and VEGFR 2. Its antagonist, soluble Flt 1 (sFlt 1), binds VEGF without promoting signaling, inhibiting its action.

Histological changes in GDM affected placentas include thickened placental barriers, fibrinoid necrosis, and chorangiosis. Studies measuring VEGF levels in GDM have shown inconsistent results, with some reporting increased and others decreased levels. These variations may arise from differences in cytokine states. Correlating serum VEGF levels with placental histology may offer insights and suggest VEGF as a potential therapeutic target for GDM